Conditioned taste aversion in rats with excitotoxic brain lesions

Yamamoto, Takashi; Fujimoto, Yoshiyuki; Shimura, Tsuyoshi; Sakai, Nobuyuki

doi:10.1016/0168-0102(95)00875-t

Cited by 225 publications

(159 citation statements)

References 60 publications

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“…However, the -6 -amount of Sac intakes gradually increased toward the 3rd test day (D3: 5.9 ± 1.5 ml) as shown in previously reports [3,5,6,10,15,33]. When CS was paired with saline instead of LiCl, CTA was never induced, and rather significant increase of Sac intake was observed on the 2nd to 3rd test day rather than decreaseas shown in our previous paper [15].…”

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confidence: 82%

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Effects of midazolam on acquisition and extinction of conditioned taste aversion memory in rats

Ayuse

Yoshida

et al. 2009

Neuroscience Letters

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Some intravenous anesthetic agents such as midazolam are known to induce anterograde and retrograde amnesia. We analysed the effect of midazolam by the conditioned taste aversion (CTA) acquisition and retention. After the rats were offered 0.1% sodium saccharin (Sac) as conditioned stimulus (CS), an intraperitoneal (i.p.) injection of several concentrations (5 ~ 30 mg/kg) of midazolam was followed by an i.p. injection of 0.15 M LiCl (2% of body weight) as unconditioned stimulus (US). The rats, which acquired CTA by every CS-US paradigm, strongly avoided Sac on the 1st test day after conditioning and maintained the avoidance for 3 days. We have already reported that Sac intake abruptly increased on the 2nd test day and the almost complete extinction occurred on the 3rd test day after conditioning by injection of subhypnotic dose of propofol before LiCl-injection. In contrast, we found that subhypnotic dose of midazolam suppressed not only CTA acquisition, but also CTA retention. On the other hand, an α2-adrenergic blocker, yohimbin (1 mg/kg) suppressed only the CTA retention. These results suggest that the subhypnotic doses of midazolam firstly affect the acquisition mechanism of the CTA memory (CTAM ), resulting the suppression of the retention of CTAM.Key words: midazolam ; CTA; memory; acquisition; extinction; amnesia, Yohimbin, noradrenergic system -3 -Intravenous anesthetics such as midazolam, one of benzodiazepine anesthetic agents, which possess both γ-aminobutylic acid (GABA)-like [13,29], are known to induce anterograde and retrograde amnesia in human [16,17] and rodents [24,26]. In rodents, it has been reported that anterograde amnesia of an avoidance task was elicited by subhypnotic doses of the intravenous anesthetics, but retrograde amnesia was induced merely by hypnotic doses of these anesthetics [24,25,27].Previous works using a CTA paradigm, where conditioned taste aversion memory (CTAM) related to malaise is formed when an animal consumes a novel taste such as saccharin (conditioned stimulus, CS) and then experiences the symptoms of poisoning such as LiCl (unconditioned stimulus, US) [9], show that the strong CTA is established rapidly by novel taste stimuli in a single learning procedure [5,32]. The association between the CS and the US can proceed under deep anesthesia induced by pentobarbital or ketamine when hypnotic doses of these anesthetics are administrated after CS-presentation, or subhypnotic doses of them, which do not impair drinking, was applied before CS-presentation [6,33].However, subhypnotic doses of the intravenous anesthetics are often used for disabled patients even in light operation such as extraction of teeth to sedate their hyperactivity [22,31]. We often encounter patients, who have lost the memory during operation after administration of sedative dose of these intravenous anesthetics while they preserved their consciousness during operation [22]. In the previous paper [15], we reported that subhypnotic but not hypnotic doses of propofol, one of non-benzodiazepine...

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confidence: 82%

“…The association between the CS and the US can proceed under deep anesthesia induced by pentobarbital or ketamine when hypnotic doses of these anesthetics are administrated after CS-presentation, or subhypnotic doses of them, which do not impair drinking, was applied before CS-presentation [6,33].…”

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confidence: 99%

Effects of midazolam on acquisition and extinction of conditioned taste aversion memory in rats

Ayuse

Yoshida

et al. 2009

Neuroscience Letters

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“…Other structures that have been implicated in the formation of a CTA include the hypothalamus (Roth et al, 1973), basal forebrain (Lopez-Garcia et al, 1993) and potentially the noradrenergic system (Dunn and Everitt, 1987). Lesions of the hippocampus impact CTA only mildly, or not at all (Best and Orr, 1973, Murphy and Brown, 1974, Yamamoto et al, 1995. Therefore, CTA appears to be an ideal paradigm for evaluating non-spatial forms of learning, not dependent on hippocampal function, in mouse models of AD.…”

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confidence: 99%

Acquisition of conditioned taste aversion is impaired in the amyloid precursor protein/presenilin 1 mouse model of Alzheimer’s disease

2008

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Research into the underlying mechanisms of cognitive dysfunction in Alzheimer's disease (AD) has relied traditionally on tasks such as the water maze which evaluate spatial learning and memory. Since non-spatial forms of memory are also disrupted by AD, it is critical to establish other paradigms capable of investigating these deficits. Utilizing a non-spatial learning task, acquisition of conditioned taste aversion (CTA) was evaluated in a mouse model of AD. This line of transgenic mice encode a mutated allele of the human amyloid precursor protein (APP) and presenilin 1 (PS1) genes and exhibit extensive amyloid plaque deposition in the brain by 6-7 mo of age. Compared to wildtype mice, 10-17 month old APP/PS1 mice failed to acquire CTA to saccharin. Mice that only possessed one of the two mutations were able to acquire CTA to the saccharin. In 2-5 month old APP/PS1 mice acquisition of CTA was disrupted despite the lack of extensive plaque deposition. However, further analysis indicated a potential gender difference in both the CTA deficit and onset of plaque deposition with females showing greater conditioned aversion.Alzheimer's disease (AD) is one of the most prominent neurodegenerative disorders associated with aging. The hallmark symptom of AD is impaired learning and memory function that progresses from mild to severe. AD is characterized pathologically by extra-cellular deposition of beta-amyloid (Aβ) plaques and intra-cellular neurofibrillar tangles consisting of aggregrates of hyperphosphorylated protein tau (Selkoe, 1989, Mandelkow andMandelkow, 1998). The pathology is first observed in the hippocampal and cortical regions and has been shown to be correlated with deficits in learning and memory , although this linkage remains controversial (Morgan, 2003).Over the past decade the use of mice expressing human familial mutations of AD has provided insight into the relationship between the pathological mechanisms and memory impairments (Ashe, 2001). Mice expressing mutations in amyloid precursor protein (APP), presenilin-1 (PS1), presenilin-2 (PS2), tau or apolipoprotein (apoE) have been generated to model various behavioral physiological, pathological and biochemical aspects of AD (Corder et al., 1998, Ashe, 2000, Lewis et al., 2001, Gordon et al., 2002, Hwang et al., 2002, Jolas et al., 2002, Teter et al., 2002. The mice developed thus far to investigate the pathology and learning and memory associated deficits in AD do not include a mouse that possesses all of the 1 Correspondence: Dr. Paul J. Pistell, Nutritional Neuroscience and Aging Laboratory, Pennington Biomedical Research Center, 6400 Perkins Rd., Baton Rouge, Louisiana 70808, Tel: 225/763-2739, Fax: 225/763-0261, Email:Paul.Pistell@pbrc.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is pub...

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“…Some studies have reported that VPMpc-lesioned animals retain a normal concentration response to preferred and non-preferred tastes [134][135][136][137] but may have disrupted [137], impaired [127,130] or else have no effects on CTA [134,135,138,139]. Current views suggest a role in comparing novel and familiar tastes [140] in more complex gustatory learning tasks or in attention to gustatory function [135,136,141].…”

Section: The Gustatory System In the Ratmentioning

confidence: 99%

“…Lesions on either the medial or lateral parts of the nucleus disrupt taste preference [120,124], selective neophobia [125,126], sodium appetite [127,128] and CTA [121,[126][127][128][129][130].…”

Section: The Gustatory System In the Ratmentioning

confidence: 99%